The emergence of Zika virus (ZIKV) in Central America in 2015 coincided with a surge in the incidence of microcephaly. A growing body of epidemiological and experimental evidence strengthens the assumption that prenatal ZIKV infection causes microcephaly.
This project aims at characterizing the pathogenicity of ZIKV in neurologically relevant cells. Furthermore, it is still an open question, whether Zika isolates from Africa versus Asia/South America differ in their pathogenicity.
We have a collection of ZIKV strains from recent outbreaks in Polynesia and Central America and from endemic areas in Africa. Additionally, we have different cell cultures systems for neurologically relevant cell types. With these experimental systems, we will elucidate whether specific ZIKV strains differ in their pathogenicity and we will characterize underlying molecular mechanisms.
This project will provide a contribution to understanding the impact of ZIKV infection on brain development, which is required for prophylactic and therapeutic approaches against the sequelae of the global ZIKV epidemics.
Accumulating epidemiological evidence and data from in vitro models of human brain development suggest that prenatal Zika virus infection causes severe fetal brain malformations, including microcephaly. Virological aspects as well as the cellular and molecular mechanisms of the impact of ZIKV infection on brain development need to be characterized in order to assess target-oriented prophylactic and/or therapeutic approaches to prevent ZIKV-induced fetal malformations in the future.
Inst. for Med. Microbiology, Immunology and Hygiene
Executive Board Member assoc. CMMC Research Groupshow more…